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Mechanism of Cardiac Arrhythmias

Mechanism of Cardiac Arrhythmias

Arrhythmias are irregular heart rhythms occurring when the heart's electrical impulses become abnormal. These disturbances can lead to various symptoms, depending on their severity and the underlying cause. Some common factors contributing to arrhythmias include hypoxia, ischemia, electrolyte imbalances, excessive catecholamine exposure, drug toxicity, and muscle overstretching. Arrhythmias can be classified into two main types based on the rate and site of origin of abnormal heart rhythms.

Antiarrhythmic Drugs: Class I Agents as Sodium Channel Blockers

Antiarrhythmic Drugs: Class I Agents as Sodium Channel Blockers

Class I antiarrhythmic drugs are used to treat various types of arrhythmias or irregular heart rhythms. These drugs block the sodium (Na+) channels in the cardiac cells, thereby affecting the movement of electrical impulses across the heart. Class I antiarrhythmic drugs are divided into three subgroups: Class IA, Class IB, and Class IC, each with distinct mechanisms of action and effects on the heart.
Class 1A Antiarrhythmic Drugs: These drugs work by moderately blocking sodium channels,...

Antiarrhythmic Drugs: Class II Agents as β-Adrenergic Blockers

Antiarrhythmic Drugs: Class II Agents as β-Adrenergic Blockers

Adrenergic stimulation generally impacts cardiac rate and rhythm. Specifically, stimulation of the β-adrenoceptors triggers an increase in intracellular calcium ion influx and pacemaker currents, which may cause arrhythmias. Catecholamines like adrenaline also demonstrate β2-adrenoceptor-mediated hypokalemia, impacting cardiac action potential and disrupting the normal cardiac rhythm. Class II antiarrhythmic drugs are β-adrenoceptor antagonists or β-blockers, which indirectly block calcium...

Antiarrhythmic Drugs: Class III Agents as Potassium Channel Blockers

Antiarrhythmic Drugs: Class III Agents as Potassium Channel Blockers

Class III antiarrhythmic drugs are a group of medications that can prolong action potentials in the heart. They achieve this by blocking potassium channels or enhancing inward currents from sodium channels. However, these drugs have a unique property of "reverse use-dependence," which is most pronounced at slower heart rates and can lead to torsades de pointes—a specific type of arrhythmia. However, it is essential to note that excessive QT interval prolongation—a measure of the heart's...

Disturbances in Heart Rhythm

Disturbances in Heart Rhythm

Arrhythmia or dysrhythmia refers to an abnormal heart rhythm caused by a defect in the heart's conduction system. It can cause the heart to beat irregularly, too quickly, or too slowly, leading to symptoms like chest pain, shortness of breath, and fainting. Factors such as stress, caffeine, alcohol, nicotine, cocaine, certain drugs, congenital defects, diseases, and electrolyte abnormalities can trigger arrhythmias.
Arrhythmias are categorized by their speed, rhythm, and origin. A slow heart...

Dysrhythmias VI: Management of Dysrhythmias

Dysrhythmias VI: Management of Dysrhythmias

Dysrhythmia management involves a multifaceted approach, incorporating pharmacological treatments, medical procedures, surgical interventions, lifestyle modifications, and patient education.Pharmacological ManagementAntiarrhythmic Drugs:Class I (Sodium Channel Blockers): This class includes quinidine and procainamide, which reduce the speed of impulse conduction in the heart, stabilize the cardiac membrane, and control arrhythmias. Quinidine and procainamide are Class IA agents that prolong the...

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Related Experiment Video

Updated: Jul 14, 2026

Methods for ECG Evaluation of Indicators of Cardiac Risk, and Susceptibility to Aconitine-induced Arrhythmias in Rats Following Status Epilepticus

Methods for ECG Evaluation of Indicators of Cardiac Risk, and Susceptibility to Aconitine-induced Arrhythmias in Rats Following Status Epilepticus

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Drug-induced proarrhythmia: Discussion and considerations for clinical practice.

Ralph J Klotzbaugh¹, Alejandra Martin², John Rick Turner³

¹University of New Mexico College of Nursing, Albuquerque, New Mexico.

Journal of the American Association of Nurse Practitioners

|February 5, 2020

Summary

This article discusses drug-induced proarrhythmia, focusing on Torsade de Pointes (Torsade). QT interval prolongation on ECG is a biomarker for Torsade risk, informing drug safety and prescribing information.

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Area of Science:

Pharmaceutical Medicine
Clinical Pharmacology
Cardiology

Background:

Drug safety is crucial in pharmaceutical medicine.
Drug-induced proarrhythmia, specifically Torsade de Pointes (Torsade), poses a significant risk.
Torsade can lead to serious adverse events, including sudden cardiac death.

Purpose of the Study:

To discuss drug-induced proarrhythmia and Torsade de Pointes.
To explain the role of QT interval prolongation as a biomarker for Torsade risk.
To review the assessment of drug proarrhythmic potential during clinical development.

Main Methods:

Utilized clinical pharmacology studies during drug development.
Assessed drug propensity to induce Torsade via QT interval prolongation on ECG.
Reviewed drug benefit-risk balance for marketing approval.

Main Results:

QT interval prolongation is a key biomarker for Torsade risk.
Identification of QT prolongation does not always preclude marketing approval.
Drugs with QT prolongation risk may receive approval with prescribing warnings.

Conclusions:

Understanding drug-induced proarrhythmia is vital for patient safety.
The QT interval serves as a critical indicator in assessing drug-related cardiac risks.
Benefit-risk assessment guides regulatory decisions for proarrhythmic drugs.